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Journal of Biomedicine and Biotechnology
Volume 2005 (2005), Issue 2, Pages 189-197
Research article

Cardiovascular Damage in Alzheimer Disease: Autopsy Findings From the Bryan ADRC

1Center for Demographic Studies, Duke University, 2117 Campus Drive, Box 90408, Durham, NC 27708-0408, USA
2Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA
3Division of Pathology, Duke University Medical Center, Durham, NC 27710, USA
4Division of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA
5Soybean Genomics and Improvement Laboratory, USDA-ARS, Beltsville, MD 20705, USA

Received 7 June 2004; Revised 29 November 2004; Accepted 7 December 2004

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Autopsy information on cardiovascular damage was investigated for pathologically confirmed Alzheimer disease (AD) patients (n=84) and non-AD control patients (n=60). The 51 relevant items were entered into a grade-of-membership model to describe vascular damage in AD. Five latent groups were identified “I: early-onset AD,” “II: controls, cancer,” “III: controls, extensive atherosclerosis,” “IV: late-onset AD, male,” and “V: late-onset AD, female.” Expectedly, Groups IV and V had elevated APOEε4 frequency. Unexpectedly, there was limited atherosclerosis and frequent myocardial valve and ventricular damage. The findings do not indicate a strong relationship between atherosclerosis and AD, although both are associated with the APOEε4. Instead, autopsy findings of extensive atherosclerosis were associated with possible, not probable or definite AD, and premature death. They are consistent with the hypothesis that brain hypoperfusion contributes to dementia, possibly to AD pathogenesis, and raise the possibility that the APOE allele ε4 contributes directly to heart valve and myocardial damage.